Deficiency of TREK-1 potassium channel exacerbates blood-brain barrier damage and neuroinflammation after intracerebral hemorrhage in mice.
Yongkang FangYeye TianQibao HuangYue WanLi XuWei WangDengji PanSuiqiang ZhuMin-Jie XiePublished in: Journal of neuroinflammation (2019)
These results establish the first in vivo evidence for the protective role of TREK-1 in blood-brain barrier injury and neuroinflammation after intracerebral hemorrhage. TREK-1 may thereby be harnessed to a potential therapeutical target for the treatment of intracerebral hemorrhage.
Keyphrases
- blood brain barrier
- cerebral ischemia
- brain injury
- traumatic brain injury
- lipopolysaccharide induced
- subarachnoid hemorrhage
- lps induced
- cognitive impairment
- oxidative stress
- replacement therapy
- inflammatory response
- combination therapy
- high fat diet induced
- skeletal muscle
- risk assessment
- adipose tissue
- insulin resistance
- climate change